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I agree with Dr. Augoustides that my review article1 “does not detail the role of venous pressure in spinal cord perfusion.” The review is focused “on the gross physiologic relation within the venous system.”1(p735)Therefore, I did not discuss the role of veins in different organs and systems. Nevertheless, the issue per se
is quite important. The spinal cord injury during surgical repair of thoracoabdominal aneurysms to a great extent depends on a dramatic decrease in spinal cord perfusion pressure, which is defined as a difference between distal aortic pressure minus cerebrospinal fluid pressure or venous pressure, whichever is higher. It is clear from this simple equation that the higher the central venous pressure (CVP) is, the lower perfusion pressure would be. The work by Etz et al.2 quoted by Dr. Augoustides does not prove but is in agreement with the speculation above. Their and other observations strongly suggest that a high CVP can be dangerous for this patient population. Interestingly, similar situations can be observed in patients undergoing liver transplantation: A high CVP may jeopardize the perfusion of the transplanted liver. Therefore, I agree with Dr. Augoustides that increased intramural and transmural CVP can be detrimental to perfusion of quite a few organs, including the spinal cord. Finally, I thank Dr. Augoustides for high evaluation of my review article.

I am very thankful to Dr. Jayant for bringing to our attention an excellent and innovative work by Brengelmann.3,4 Compared with the classic work of Guyton, Brengelmann and also Levy5 have introduced an interesting and important concept emphasizing the role of the heart as a pump and shifts of blood volume within the circulatory system. Regarding the volume shifts, the discussion of the flow–pressure–volume relation in figure 3 of the review1(p737)as well as the two-compartment model(pp739–41)address this issue. Regarding pump function, Levy and Brengelmann are correct in that it is crucially important that circulation stop without a pump. The Guyton concept of mean circulatory filling pressure (MCFP) is not necessarily incorrect: Stress volume and pump function are needed to maintain MCFP, and only then (when it is maintained by stress volume and pump function) does MCFP become the driving force for venous return. This is why Rothe6 declared that the MCFP is the “pivoting pressure,” emphasizing the importance of this pressure as a driving force for venous return.

At the end of his first paragraph, Dr. Jayant correctly says that “failure of pump function leads to an assortment of chemical mediators that can … affect the venous capacity.” I agree. In the second paragraph of the letter, Dr. Jayant expresses the thought that analysis of the overall circulatory system “that stops at the right atrium is seemingly not complete.” I also agree. The review in question focuses only on the venous system,1(p735)not on “the overall circulatory system.” The fact that the review does not discuss in detail heart and pulmonary circulation should not be construed to say that I do not believe that these parts of the circulation are important. The review describes the venous system itself in more detail than the work by Levy and Brengelmann does; the latter focuses more on the overall cardiovascular system than on the details of the venous system per se
. If I had introduced the concept described by Brengelmann, I would have had to delete something else that in my mind is more relevant to the focus of the review.

In the third paragraph of his letter, Dr. Jayant says that the two-compartment model described in my review “offers an elegant explanation of the increase in filling pressure with aortic clamping.” Then Dr. Jayant says that “as the physiologic setting becomes complex (heart failure …) it becomes increasingly difficult to apply.” Not at all. As I mentioned in my review,1(p737)a decrease in cardiac output due to cardiac failure would decrease flow from the splanchnic arteries, decrease volume within splanchnic veins, and shift this volume to the systemic circulation, increasing preload and recruiting the Frank–Starling mechanism.

A few lines later, I am afraid Dr. Jayant does not properly distinguish the two compartments within the venous system: “working like an arteriovenous fistula” in my example is related to a decrease in arterial resistance in the fast (main) compartment rather than to a decrease in resistance to hepatic outflow (slow compartment). Despite that these specific examples that Dr. Jayant lists in this paragraph fit quite well (and can be easily explained by) the two-compartment model, I agree conceptually that not all physiologic and pathophysiologic observations can fit this model. Models rarely if ever explain everything.

In the same paragraph, Dr. Jayant separates changes in stress volume from the mobilization of this volume; then he says, “This is an either/or function.” I disagree. This is the same function: Mobilization of blood volume from the splanchnic system is an increase in stress volume secondary to the shift of blood from unstressed volume.

In the fourth paragraph of his letter, Dr. Jayant writes that “increased intrathoracic pressure increases transmural central venous pressure.” This is wrong in most situations and is certainly wrong in the situation when an increase in intrathoracic pressure is due to routine controlled ventilation in a patient with normal heart function and blood volume. In such a situation, transmural CVP does not increase; only intramural CVP does. When intramural CVP is increased, the sympathetic nervous system is moderately activated, leading to an increase in splanchnic arterial resistance (associated with a passive recoil of splanchnic veins) as well as active constriction of the splanchnic veins (veins are much more sensitive to sympathetic stimulation than arteries),7 working in concert with squeezing the abdominal venous system by the shift of the diaphragm downward and increasing intraabdominal pressure. These responses increase stressed volume and then MCFP, which maintains the baseline pressure gradient for venous return (MCFP − CVP). This does not lead, as Dr. Jayant suggests, to splanchnic ischemia. If it did, we would be dead before we started walking: Every time we stand up, a low degree of sympathetic stimulation occurs, and blood shifts from the splanchnic veins into the systemic circulation to increase stress volume and MCFP, maintaining normal transmural CVP and venous return. Only a high degree of sympathetic nervous tone might lead to severe arterial constriction within the splanchnic vasculature, which might jeopardize blood supply to the gut. Dr. Jayant writes “most would agree that significant abdominal hypertension calls for only one therapeutic modality: early abdominal decompression.” I disagree only with the word most
: I would say that all
would agree with this notion. Therefore, the whole point here is the degree of increase in sympathetic nervous system discharge: A low degree is absolutely needed for every moment of survival, whereas a high degree is dangerous.1(pp739,741,744)

Finally, I am happy that Dr. Jayant, having a very critical mind, agrees with me that “increased central venous pressure is still a useful clinical tool in the evaluation of right heart or pericardial disease”; I say so in the review.(p744)Therefore, I would not think that my review is a requiem to the CVP; it is rather an opera; opera
in Latin means “labor” or “work produced,” where many parts (singing, dancing, visual art, music, and so on) are put together.8

We should be thankful to Dr. Tavernier et al.
for sharing with us their recent observations on the importance of an increase in pulse pressure (deltaPP-up) compared with an increase in systolic pressure (delta-up), mentioned in my review.1 In the review, I was talking about both systolic pressure variation (SPV) and pulse pressure variation (PPV). I started the description with delta-up; however, just a few lines later I wrote about delta-down, mentioning that it is larger than delta-up and referring to the total SPV: delta-up plus delta-down. In SPV, delta-down plays a more important role than delta-up does, not only because it is larger but also because it reflects the volume status, as was shown by Dr. Tavernier et al.
a decade ago.9 Practically, it is much easier to assess SPV than PPV. I agree that PPV is considered to be a more accurate indicator of responsiveness to fluid load than SPV is; however, the differences between them are really minimal.10 For example, a relatively recent study demonstrated that the coefficients of correlation between stroke volume and SPV or PPV were exactly the same: 0.91.11

Other investigators also found that SPV and PPV were the most accurate predictors of fluid responsiveness, even emphasizing that SPV was more independent of the setting of mechanical ventilation.12 Therefore, mainly based on the simplicity and usefulness of using the SPV, this section of the review1 addressed the SPV as a total, with the main component of delta-down rather than focusing only on delta-up. Obviously, I would echo the opinion of Dr. Tavernier et al.
that if one has an opportunity in clinical practice to assess PPV with separation of deltaPP-up and deltaPP-down, it would ensure more accurate assessment of patient’s volume status.